Morphometric and ultrastructural changes with ageing in mouse peripheral nerve

Qualitative and quantitative information is reported on the morphological changes that occur in nerve fibres and nonneuronal cells of peripheral nerve during the lifetime of the mouse. Tibial nerves of mice aged 6–33 mo were studied. With ageing, collagen accumulates in the perineurium and lipid droplets in the perineurial cells. Macrophages and mast cells increase in number, and onion bulbs and collagen pockets are frequently present. Schwann cells associated with myelinated fibres (MF) slightly decrease in number in parallel with an increase of the internodal length from 6 to 12 mo, but increase in older nerves when demyelination and remyelination are common. The unmyelinated axon to myelinated fibre (UA/MF) ratio was about 2 until 12 mo, decreasing to 1.6 by 27 mo. In older mice, the loss of nerve fibres involves UA (50% loss of 27–33 mo cf. 6 mo) more markedly than MF (35%). In aged nerves wide incisures and infolded or outfolded myelin loops are frequent, resulting in an increased irregularity in the morphology of fibres along the internodes. In the mouse there is an adult time period, 12–20 mo, during which several features of degeneration progressively appear, and an ageing period from 20 mo upwards when the nerve suffers a general disorganisation and marked fibre loss.

Autogenous artery grafts in hypertensive (SHR) rats do not have increased smooth muscle cell hyperplasia in the graft neointima, compared with grafts in normotensive rats

Vein-to-artery graft surgery is used widely to by-pass arterial stenoses, but such grafts can fail over a prolonged period as a result of excessive neointimal hyperplasia causing thrombosis and graft occlusion. It has been suggested that neointimal hyperplasia, in vein grafts, is a result of the vessel wall adapting to the higher intraluminal pressure of the arterial circulation, compared with the venous circulation. Autologous artery grafts have been used to bypass arterial stenoses. Initially it was assumed that donor artery segments would not develop neointimal hyperplasia as they are already adapted to the arterial circulation but this is not so. In this study we postulated that surgical or postsurgical trauma was the cause of neointimal hyperplasia in autologous artery-to-artery grafts. In addition, as artery grafts are pre-adapted to the arterial circulation, autologous artery-to-artery grafts in hypertensive rats should develop similar levels of neointimal hyperplasia as seen in normotensive rats. Artery-to-artery grafts were placed in a series of 20 spontaneously hypertensive rats (SHR). In a separate series of sham grafting experiments the effects of anoxia and clamp trauma were assessed in SHR and WKy normotensive control rats. Finally, clamping, anoxia and anastomosis trauma were assessed in a similar series of rats. In the artery-to-artery graft series there was no difference in neointimal thickness between the SHR and that previously reported for normotensive rats. Minimal neointimal hyperplasia was demonstrated in the sham grafted series of rats and only slightly more in the single anastomosis series. It was only in the full grafting procedure that considerable neointimal hyperplasia developed. These data demonstrate that neointimal hyperplasia in artery-to-artery grafts is not exacerbated by the hypertension. In addition, trauma appears to be the initiator of neointimal hyperplasia and the extent of trauma correlates with the degree of neointimal hyperplasia.

Postnatal development of intestinal endocrine cell populations in the water buffalo

The frequency and distribution of 11 endocrine cell populations were studied in the intestine of differently aged buffalo, grouped on the basis of diet: 2-d-olds (suckling), 5-mo-olds (weaning) and 5-y-olds (ruminant adult diet). The endocrine cell populations were identified immunocytochemically using antisera against 5-hydroxytryptamine (5-HT), somatostatin, gastrin, cholecystokinin (CCK), COOH-terminal octapeptide of gastrin/CCK, neurotensin, motilin, gastric inhibitory polypeptide (GIP), secretin, glucagon/glicentin (GLU/GLI) and polypeptide YY (PYY). In adult buffalos the regional distribution of endocrine cells is similar to that of other adult ruminants. During postnatal development, these cell types showed the following changes in their frequency and distribution: (1) 5-HT, neurotensin and gastrin/CCK immunoreactive cells (i.c.) showed a decrease in frequency with age; (2) somatostatin i.c. frequency remained stable with age; (3) motilin, GIP, secretin and CCK i.c. showed a slight increase in frequency with age; (4) GLU/GLI and PYY i.c. decreased in frequency with age in the small intestine, caecum and proximal colon and an increase in frequency in the rectum. It was hypothesised that the endocrine cell types, whose presence and localisation is substantially stable in all examined ages, probably contain substances that are strictly necessary for intestinal function. In contrast the hormones contained in the cell populations that decreased with age, are probably involved in physiological needs during the milk and weaning diet or play a role in intestinal growth.

Structural abnormalities do not explain the early functional abnormalities in the peripheral nerves of the streptozotocin diabetic rat

The streptozotocin (STZ)-diabetic rat, the most commonly employed model of experimental diabetic neuropathy, is characterised by a reduction in nerve conduction velocity, pain threshold and blood flow. Whether or not structural abnormalities underlie these functional abnormalities is unclear. 10 adult male Sprague–Dawley STZ-diabetic rats (diabetes duration 27 d) and 10 age-matched (23 wk) control animals were studied. Motor nerve conduction velocity (m s−1) was significantly reduced in diabetic (41.31±0.8) compared with control (46.15±1.5) animals (P<0.001). The concentration of sciatic nerve glucose (P<0.001), fructose (P<0.001) and sorbitol (P<0.001) was elevated, and myoinositol (P<0.001) was reduced in diabetic compared with control animals. Detailed morphometric studies demonstrated no significant difference in fascicular area, myelinated fibre density, fibre and axon areas as well as unmyelinated fibre density and diameter. Endoneurial capillary density, basement membrane area and endothelial cell profile number did not differ between diabetic and control animals. However, luminal area (P<0.03) was increased and endothelial cell area (P<0.08) was decreased in the diabetic rats. We conclude there is no detectable structural basis for the reduction in nerve conduction velocity, pain threshold or blood flow, observed in the streptozotocin diabetic rat.